Role of guard-cell ABA in determining maximal stomatal aperture and prompt vapor-pressure-deficit response

Abstract Abscisic acid (ABA) is known to be involved in stomatal closure. However, its role in stomatal response to rapid increases in the vapor pressure deficit (VPD) is unclear. To study this issue, we generated guard cell (GC)-specific ABA-insensitive Arabidopsis plants (GC-specific abi1-1 ; GCabi). Under normal conditions, the stomatal conductance (g s ) and apertures of GCabi plants were greater than those of control plants. This supports GC ABA role as limiting maximal stomatal aperture under non-stressful conditions. When there was a rapid increase in VPD (0.15 to 1 kPa), the g s and stomatal apertures of GCabi decreased in a manner similar that observed in the WT control, but different from that observed in WT plants treated with fusicoccin. Low VPD increased the size of the stomatal apertures of the WT, but not of GCabi. We conclude that GC ABA does not play a significant role in the initial, rapid stomatal closure that occurs in response to an increase in VPD, but is important for stomatal adaptation to ambient VPD. We propose a biphasic angiosperm VPD-sensing model that includes an initial passive-hydraulic, ABA-independent phase and a subsequent ABA-dependent steady-state phase in which stomatal behavior is optimized for ambient VPD conditions. Highlight Guard-cell ABA does not play a significant role in the immediate closure of stomata following an increase in the VPD, but is important for stomatal adaptation to ambient VPD.